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원무호 동국대학교 의학연구소 2000 東國醫學 Vol.7 No.-
This study was carried out to the effect of neuronal degeneration in the anterior horn after spinal cord ischemia. White rabbits (2.5-3 kg) were used in this study as control and experimental groups. Spinal cord ischemia was induced by occlusion of the abdominal aorta located underneath the left renal artery for 15 minutes. Subsequently, the animal were sacrified at 0.5, 1, 3, 6, 12 and 24 hours after the ischemic injury. Spinal cord sections at the level of L7 were stained with Cresyl violet and Acid fuchsin. The results obtained from the studies are as follows. The number of Cresyl violet-positive neurons began to be reduced in the laminae IX 3 hours after ischemia. In contrast, the Cresyl violet-positive neurons in the laminae Ⅶ and Ⅷ began to be decreased 6 hours after ischemia. Finally, no neurons could be detectable with Cresyl violet 24 hr after the ischemic injury. These result suggest that the neuronal degeneration in the anterior horn may occur rapidly after ischemic insults at normothermic condition.
Post-ischemic Time-dependent Activity Changes of Hippocampal CA1 cells of the Mongolian Gerbils
원무호,신형철 대한약리학회 2007 The Korean Journal of Physiology & Pharmacology Vol.11 No.6
Changes of single unit activity of CA1 hippocampus region were investigated in anesthetized Mongolian gerbils for six days following transient ischemia. Ischemia was produced immediately before the implantation of micro-wire recording electrodes. In control animals receiving pseudo-ischemic surgery, neither spontaneous neuronal activities (5.70±0.4 Hz) nor the number of recorded neurons per animal changed significantly for six days. Correlative firings among simultaneously recorded neurons were weak (correlation coefficient >0.6) in the control animals. Animals subjected to ischemia exhibited a significant elevation of neural firing at post-ischemic 12 hr (9.95±0.9 Hz) and day 1 (8.48± 0.8 Hz), but a significant depression of activity at post-ischemic day 6 (1.84±0.3 Hz) when compared to the activities of non-ischemic control animal. Ischemia significantly (correlation coefficient <0.6) increased correlative firings among simultaneously recorded neurons, which were prominent especially during post-ischemic days 1, 2 and 6. Although the numbers of spontaneously active neurons recorded from control group varied within normal range during the experimental period, those from ischemic group changed in post-ischemic time-dependent manner. Temporal changes of the number of cells recorded per animal between control group and ischemic group were also significantly different (p = 0.0084, t = 3.271, df = 10). Cresyl violet staining indicated significant loss of CA1 cells at post-ischemic day 7. Overall, we showed post-ischemic time-dependent, differential changes of three characteristics, including spontaneous activity, network relationship and excitability of CA1 cells, suggesting sustained neural functions. Thus, histological observation of CA1 cell death till post-ischemic day 7 may not represent actual neuronal death.